Seed development begins upon double fertilization, producing the embryo and endosperm, which are genetically identical, except for their ploidy level. DEMETER (DME), a member of the DNA glycosylase family, functions as a DNA demethylase via the base excision repair pathway. DME is specifically expressed prior to fertilization in two gamete companion cells, central cell of the female gametophyte and vegetative cell of the male gametophyte, but not in the heritable gamete cells or embryo. Mutations in the DME gene cause hypermethylation in the endosperm, leading to endosperm overproliferation and seed abortion after fertilization. DME-mediated DNA demethylation preferentially targets euchromatic transposable elements (TEs), resulting in TE activation and initiation of de novo methylation through RNA-directed DNA methylation, and provides FERTILIZATION-INDEPENDENT SEED 2 (FIS2)-Polycomb Repressive Complex 2-binding sites, resulting in histone modifications and genomic imprinting during reproduction. The global demethylation of TEs in gamete companion cells and active de novo methylation in the embryo suggest a new role of sexual companion cells in reinforcing the genome integrity of the heritable tissue. In this review, we provide an overview of demethylation in sexual companion cells and the endosperm, and discuss its evolutionary effect on the heritable gamete cells and embryo.

种子的发育从双重受精开始，产生胚胎和胚乳，除了倍性水平外，它们在遗传上是相同的。DNA糖基化酶家族的成员DEMETER（DME）通过碱基切除修复途径充当DNA脱甲基酶。DME在受精前在雌性配子体的中央细胞和雄性配子体的营养细胞这两个配子伴侣细胞中特异性表达，但在可遗传的配子细胞或胚胎中不表达。DME中的突变该基因在胚乳中引起甲基化过高，导致胚乳过度增殖并在受精后导致种子流产。DME介导的DNA去甲基化优先靶向常染色体转座因子（TEs），从而导致TE活化和通过RNA定向的DNA甲基化而引发从头甲基化，并提供了FERTILIZATION-INDEPENDENT SEED 2（FIS2）-Polycomb Repressive Complex 2-binding site，导致组蛋白修饰和复制过程中的基因组印迹。配子伴侣细胞中TEs的整体去甲基化和胚胎中的主动从头甲基化表明性伴侣细胞在增强可遗传组织的基因组完整性方面的新作用。在这篇评论中，我们概述了性伴侣细胞和胚乳中的脱甲基，